Page 127 - Concise Pathology for Exam Preparation ( PDFDrive )

112 SECTION I General Pathology

Morphology of rejection
Hyperacute rejection
(a)
Occurs minutes or hours after transplantation and leads to a cyanotic, mottled
(i)
and flaccid kidney excreting a few drops of bloody urine.
(ii)
There is a rapid accumulation of neutrophils within arterioles, glomeruli and
peritubular capillaries along with deposits of immunoglobulins and complement
in the vessel wall. EM shows endothelial injury with fibrin-plated thrombi.
(b)
Acute rejection
(i)
Occurs days, months or even years after transplant.
(ii)
Both cellular and humoral responses involved.
Features of acute cellular rejection:
- Increased serum creatinine
- Clinical signs of renal failure
- Extensive interstitial mononuclear infiltrate, oedema and haemorrhage
- Mononuclear cells in the glomerular and peritubular capillaries, which may invade
tubules to induce tubular necrosis
- Vascular endothelial injury mediated by CD81 T cells

Features of acute humoral rejection:
- Mediated primarily by the antidonor antibodies

- Characterized by the necrotizing vasculitis, endothelial cell necrosis, neutrophilic

infiltrate and deposition of immunoglobulins along with complement and fibrin
(c)
Chronic rejection
(i)
Progressive rise of serum creatinine over a period of 4–5 months is the hallmark.
It is dominated by vascular changes (dense intimal fibrosis), interstitial fibrosis,
(ii)
glomerular loss, tubular atrophy, shrinkage of renal parenchyma, interstitial infil-
trate of plasma cells and eosinophils.
Q. Differentiate between acute and chronic transplant rejection.
Ans. Differences between acute and chronic rejection are enlisted in Table 5.12.
TABLE 5.12. Differences between acute and chronic rejection
Features Acute rejection � Chronic rejection
Onset Occurs within days of transplant Occurs over months to years after a transplant
Components Acute cellular and humoral (antibody-mediated) Cell-mediated rejection characterized by progres-
rejection sive organ dysfunction
Mechanism Interstitial mononuclear infiltration by CD41 Mononuclear infiltrate with numerous plasma
and CD81 T cells, endothelial injury and an- cells and eosinophils

tibody-mediated damage
Morphology Damaged tubular epithelium, rejection vasculitis Arterioles show dense intimal fibrosis leading to
(necrotizing vasculitis, thrombosis or intimal parenchymal ischaemic injury
thickening)
Q. Write briefly on transplantation of hematopoietic cells.
Ans. Indications
• �Haematological malignancies
• �Nonhaematological cancers
• �Aplastic anaemia
• �Immunodeficiency states
• �Transplantation of genetically engineered hematopoietic stem cells useful for somatic
cell gene therapy

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